The pathogenesis of ankylosing spondylitis (AS) still remains an enigma. Although
some studies have indicated the importance of T-cells and proinflammatory
cytokines in the pathogenesis of the AS, it is still unknown whether
co-stimulatory molecule CD154 participates in the pathogenesis of AS and how its
level changes during the anti-TNF-alpha treatment of AS. This study is performed
to evaluate the expression of CD154 in peripheral blood T-lymphocytes of patients
with AS and observe the change of CD154 in etanercept-treated AS patient. We
collected the peripheral blood and clinical data from 66 AS, 30 rheumatoid
arthritis (RA) patients, and 30 healthy controls. Thirty-nine active AS patients
were enrolled in a randomized double-blind placebo-controlled trial. We followed
up 37 cases that fulfilled the ASAS20 response criteria after they finished
etanercept treatment till week 48. The percentage of CD3+CD154+ in peripheral
blood lymphocytes was evaluated by flow cytometry. We found that CD154 expression
in AS patients was significantly higher than that in healthy volunteers and RA
patients (both P < 0.001). The expressions of CD154 in AS patients at active
stage or with peripheral joint involvement were significantly higher than those
at stable stage or with axial involvement alone (P = 0.005 and 0.044,
respectively). The expression of CD154 decreased in AS patients treated with
etanercept compared with patients treated with placebo at week 6 (P < 0.001).
Compared with healthy volunteers, the expression of CD154 in 16 AS patients who
relapsed after finishing etanercept treatment was elevated again (P = 0.012).
These findings show that co-stimulatory molecule CD154 is overexpressed on
T-lymphocytes in peripheral blood of AS patients and can be down-regulated by
etanercept treatment, which suggest that CD154 might be involved in the
inflammatory evolvement of AS and might be a potential biomarker to monitor AS
disease activity and the effect of etanercept treatment.